We read the recent article on this subject with
interest(1). Reye’s syndrome an acute non-inflamatory
encephalopathy is a disease entity known in the field of medicine
since 1963, despite which a lot that is known about the disease is
yet to be conclusively proven. Many studies have been undertaken
to clarify or assert the assumptions about the syndrome; as a
result of which it is by now clear that the etiology pattern is
not universally similar and a single causative agent cannot be
implicated in the etiopathogenisis.
In the above mentioned study(1), the design is
well-conceived to estimate the extent of the disease occurrence
but the etiologies still remain as presumptious and are not
conclusive.
We would like to draw the attention of the
authors to another study done on the same subject by the Indian
Council of Medical Research in Vani Vilas Hospital in south
India(2). One hundred and twenty four cases of Reye’s syndrome
admitted to Vani Vilas children’s hospital, Bangalore, during
the period of October 1983 to December 1986 were investigated.
Clinical, biochemical and epi-demiologic details were obtained.
The median age was 5 years with no difference in sex ratio. This
disease was frequent in winter months. Cases clustered in certain
congested localities of the city among the lower socio-economic
strata. Aspirin and varicella could not be associated as preceding
factors. The clinical and biochemical features of the patients
were suggestive of Reye’s syndrome.
Histopathological evaluation was done in 104
liver biopsy specimens. Virological studies for influenza and
Arbovirus were negative. Mortality was high (78%)(2). This study
could not establish salicylates as the etiologic agent. The
practice of selling salicylates as a over-the-counter drug for
fever in children is no longer seen, atleast in the pharmacies of
major cities, strongly suggesting against aspirin as a sole
putative agent. However, it is wise to be cautious about its valid
use in the concerned clinical situations only, for example,
rheumatoid arthritis. It is premature to conclude that aspirin is
the causative agent by some circumstantial evidence like finding
aspirin in the dispensaries of practitioners surveyed.
Further, regarding the viral etiology of Reye’s
Syndrome, the study does not mention if viral isolation or serum/CSF
serology was the method employed for diagnosis and if it was the
latter (CSF serology), was it exclusively positive and if so in
how many? To implicate only measles and varicella with the data
published would be inadequate.
The study has served to estimate the extent of
Reye’s Syndrome and the awareness of the disease among
practitioners. It has also created awareness of situations where
it is deficient by health education intervention. However, it is
still inconclusive about the etiology of the disease.
D.G. Benakappa,
Vanitha J.,
Indira Gandhi Institute of Child Health,
South Hospital Complex,
Dharmaram College Post,
Bangalore 560 029, India.
References
1. Ghosh D, Dhadwal D, Aggarwal A, Mitra S,
Garg SK, Kumar R, et al. Investigation of an epidemic of Reye’s
syndrome in Northern region of India. Indian Pediatr 1999; 36:
1097-1106.
2. Benakappa DG, Das S, Shankar SK, Rama Rao BSS, George PS,
Awasth PS, et al. Reye’s syndrome in Bangalore. Indian J
Pediatr 1991; 58: 805-810.
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